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INSERM U-457 (D.J., J.L., P.C., C.L.-M.), and the Department of Hormonology and Biochemistry (D.C.), Hôpital R. Debré, 75019 Paris, France
Address all correspondence and requests for reprints to: Dr. D. Jaquet, INSERM U-457, Hôpital R. Debré, 48 boulevard Sérurier, 75019 Paris, France. E-mail: djacquet{at}infobiogen.fr
It was recently suggested that precocious pubarche associated with
subsequent functional ovarian hyperandrogenism and hyperinsulinemia
could have a common origin in reduced fetal growth. We previously
reported that young women born with intrauterine growth retardation
(IUGR: birth weight less than the third percentile) were
hyperinsulinemic and less insulin sensitive than women born with normal
birth weight. The aim of the present study was to investigate whether
these IUGR-born women demonstrated hyperandrogenism compared with
controls. Our study population was composed of 130 IUGR-born women and
150 controls, of similar age (20.6 ± 3.2 vs.
20.4 ± 2.0 yr). Hormonal contraception in terms of frequency and
medication, including antiandrogenic therapy, was identical in the 2
groups. After adjustment for hormonal contraception, being born with
IUGR had no independent effect on serum androgen concentrations. In
women who were not receiving hormonal contraception, no statistical
differences were found between IUGR-born women (n = 67) and
controls (n = 64) for
4-androstenedione
(2.26 ± 0.68 vs. 2.24 ± 0.55 ng/mL;
P = 0.76), dehydroepiandrosterone sulfate
(2294 ± 1117 vs. 2489 ± 1235 ng/mL;
P = 0.24), testosterone (0.82 ± 0.85
vs. 0.70 + 0.26 ng/mL; P = 0.80), or
serum sex hormone-binding protein concentrations (45.5 ± 28.2
vs. 53.1 ± 30.3 nmol/L; P =
0.27). In both IUGR and control groups, sex hormone-binding protein
correlated negatively with fasting insulin (r = -0.23;
P = 0.03 and r = -0.26; P
= 0.05), but serum androgen levels did not correlate with insulin. In
summary, hyperinsulinemia observed in young women born with IUGR is not
associated with hyperandrogenism. Consequently, our results do not
support the hypothesis of a common in utero programming
of hyperandrogenism and hyperinsulinemia.
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